Approach to Hyponatraemia
| Step | Assessment | Finding → Diagnosis |
|---|---|---|
| 1. Assess plasma osmolality | Normal (275–295 mOsm/kg) | Pseudohyponatraemia (hyperlipidaemia, hyperproteinaemia) |
| 2. Assess volume status | Hypovolaemic (dry) | Diarrhoea, vomiting, diuretics, Addison's, burns |
| 3. Assess volume status | Euvolaemic (normal) | SIADH, hypothyroidism, glucocorticoid deficiency |
| 4. Assess volume status | Hypervolaemic (oedematous) | Heart failure, cirrhosis, nephrotic syndrome |
Most Common Causes
- SIADH (syndrome of inappropriate ADH): most common in hospital setting (lung cancer, pneumonia, drugs, CNS disease)
- Thiazide diuretics, especially in elderly women
- Heart failure and cirrhosis: dilutional hyponatraemia
- Hypothyroidism: reduces cardiac output and free water excretion
- Polydipsia (excessive water intake): primary or psychogenic
Frequently asked questions
Should a borderline Sodium result be repeated?
Do Sodium results from two different laboratories compare directly?
Does age or sex affect the Sodium reference range?
References
The clinical information on this page is drawn from peer-reviewed sources indexed by the US National Library of Medicine. Links go to the source so you can read it yourself.
- Hyponatremia. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK470386
- Hypernatremia. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK441960
- Pseudohyponatremia. In: StatPearls. Treasure Island (FL): StatPearls Publishing. NCBI Bookshelf NBK553207
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Sodium measures water, not salt
The most common misunderstanding about this test is that a low sodium means too little salt. In almost all cases it means too much water relative to salt. This is why eating more salt is rarely the treatment for hyponatraemia, and why fluid restriction is so often part of it. Understanding sodium as a concentration rather than a quantity makes the rest of the interpretation considerably easier.
Medications that commonly cause low sodium
- Thiazide diuretics, the single most frequent drug cause, often within the first weeks of starting.
- SSRIs and SNRIs, particularly in older adults, through inappropriate ADH secretion.
- Carbamazepine and oxcarbazepine, and some antipsychotics.
- Proton pump inhibitors and NSAIDs, less commonly but recognised.
- Desmopressin, where the effect is a direct extension of how the drug works.
Why correction speed matters as much as the number
Sodium that has fallen slowly over weeks is tolerated far better than the same value reached in a day, because the brain adapts. That adaptation is also why rapid correction is dangerous: raising sodium too quickly in chronic hyponatraemia can cause osmotic demyelination, a severe and often irreversible neurological injury. For this reason correction is deliberately limited, typically to single figures per 24 hours, and is monitored with frequent repeat testing. It is a good example of a laboratory number where the trajectory is managed as carefully as the destination.
High sodium and who it affects
Hypernatraemia is less common and almost always reflects water loss without adequate replacement. It concentrates in people who cannot access or ask for water: infants, those with dementia, people who are sedated or immobile, and anyone with a reduced thirst response. It also occurs with diabetes insipidus and with osmotic losses in uncontrolled diabetes. Because thirst is such a powerful defence, a persistently high sodium in an alert person with free access to fluids is unusual and warrants explanation.